Reactome diagram viewer: data structures and strategies to boost performance

Fabregat, Antonio; Sidiropoulos, Konstantinos; Viteri, Guilherme; Marín-Garcia, Pablo; Ping, Peipei; Stein, Lincoln; D’Eustachio, Peter; Hermjakob, Henning

doi:10.1093/bioinformatics/btx752

Cited by 139 publications

(120 citation statements)

References 17 publications

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“…Gene ontology (GO) and gene functional category (GFC) analyses of upregulated and downregulated genes with Log 2 FC > 0.5 were performed using DAVID Bioinformatic (https://david. ncifcrf.gov) [60] followed by Pathway Enrichment (PE) analyses in Reactome (https://reactome.org) [61].…”

Section: Next Generation Sequencing (Ngs) Using Illumina Hiseq 2500 Rmentioning

confidence: 99%

Divergent Regulation of Myotube Formation and Gene Expression by E2 and EPA during In-Vitro Differentiation of C2C12 Myoblasts

Lacham-Kaplan

Camera

Hawley

2020

IJMS

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Estrogen (E2) and polyunsaturated fatty acids (n-3PUFA) supplements independently support general wellbeing and enhance muscle regeneration in-vivo and myotube formation in-vitro. However, the combined effect of E2 and n-3PUFA on myoblast differentiation is not known. The purpose of the study was to identify whether E2 and n-3PUFA possess a synergistic effect on in-vitro myogenesis. Mouse C2C12 myoblasts, a reliable model to reiterate myogenic events in-vitro, were treated with 10nM E2 and 50μM eicosapentaenoic acid (EPA) independently or combined, for 0–24 h or 0–120 h during differentiation. Immunofluorescence, targeted qPCR and next generation sequencing (NGS) were used to characterize morphological changes and differential expression of key genes involved in the regulation of myogenesis and muscle function pathways. E2 increased estrogen receptor α (Erα) and the expression of the mitogen-activated protein kinase 11 (Mapk11) within 1 h of treatment and improved myoblast differentiation and myotube formation. A significant reduction (p < 0.001) in myotube formation and in the expression of myogenic regulatory factors Mrfs (MyoD, Myog and Myh1) and the myoblast fusion related gene, Tmem8c, was observed in the presence of EPA and the combined E2/EPA treatment. Additionally, EPA treatment at 48 h of differentiation inhibited the majority of genes associated with the myogenic and striated muscle contraction pathways. In conclusion, EPA and E2 had no synergistic effect on myotube formation in-vitro. Independently, EPA inhibited myoblast differentiation and overrides the stimulatory effect of E2 when used in combination with E2.

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Section: Next Generation Sequencing (Ngs) Using Illumina Hiseq 2500 Rmentioning

confidence: 99%

Divergent Regulation of Myotube Formation and Gene Expression by E2 and EPA during In-Vitro Differentiation of C2C12 Myoblasts

Lacham-Kaplan

Camera

Hawley

2020

IJMS

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“…Overall signaling cascades, including the TGF-beta SMAD cascade (reproduced with permission of Reactome Pathway, Fabregat et al[184]). …”

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confidence: 99%

CD36 and CD97 in Pancreatic Cancer versus Other Malignancies

Tănase

Gheorghișan-Gălățeanu

Popescu

et al. 2020

IJMS

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Starting from the recent identification of CD36 and CD97 as a novel marker combination of fibroblast quiescence in lung during fibrosis, we aimed to survey the literature in search for facts about the separate (or concomitant) expression of clusters of differentiation CD36 and CD97 in either tumor- or pancreatic-cancer-associated cells. Here, we provide an account of the current knowledge on the diversity of the cellular functions of CD36 and CD97 and explore their potential (common) contributions to key cellular events in oncogenesis or metastasis development. Emphasis is placed on quiescence as an underexplored mechanism and/or potential target in therapy. Furthermore, we discuss intricate signaling mechanisms and networks involving CD36 and CD97 that may regulate different subpopulations of tumor-associated cells, such as cancer-associated fibroblasts, adipocyte-associated fibroblasts, tumor-associated macrophages, or neutrophils, during aggressive pancreatic cancer. The coexistence of quiescence and activated states in cancer-associated cell subtypes during pancreatic cancer should be better documented, in different histological forms. Remodeling of the local microenvironment may also change the balance between growth and dormant state. Taking advantage of the reported data in different other tissue types, we explore the possibility to induce quiescence (similar to that observed in normal cells), as a therapeutic option to delay the currently observed clinical outcome.

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“…The stromal fibroblast subtype T2 predominantly expressed nine ECM-related genes (Ecm1-extracellular matrix protein 1, Fbln5-fibulin 5, Fbn1-fibrillin 1, Fndc1-fibronectin type III domain containing 1, Igfbp5-insulin like growth factor binding protein 5, Nov/Ccn3-cellular communication network factor 3, Pcolce2-procollagen C-endopeptidase enhancer 2, Col14a1-collagen type XIV alpha 1, Aspn-asporin) when compared to other stromal fibroblast subtypes ( Figure 5A), suggesting that this fibroblast subtype plays a key role in supplying these ECM components and regulatory factors in mammary glands. To determine the biological functions of these five distinct stromal fibroblasts, we performed gene pathway enrichment analysis of differentially expressed genes in these five fibroblast subtypes using the Reactome [37]. We selected differentially expressed genes based on the criteria of log2(fold change) > 0.5 and adjusted p value (FDR) < 0.001.…”

Section: High-fat Diets Induce Obesity In Brca1−/−; P53+/− Mice For Smentioning

confidence: 99%

Single-Cell RNA-seq Reveals Obesity-Induced Alterations in the Brca1-Mutated Mammary Gland Microenvironment

Yao

Zhou

2020

Cancers

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Clinical and experimental studies have shown that obesity increases the development and progression of breast cancer. The impact of obesity on the tumor microenvironment plays an important role in tumorigenesis, yet the precise mechanisms underlying obesity-mediated effects on cell-to-cell communication within the tumor microenvironment have been difficult to define. In this study, we conducted single-cell RNA sequencing (scRNA-seq) studies to investigate the impact of high-fat diet (HFD)-induced obesity on transcriptomic landscapes of stromal and immune cells in mammary glands of Brca1−/−; p53+/− mice, an animal breast cancer model. Hierarchical clustering and gene pathway enrichment analyses of scRNA-seq data showed that five different subtypes of stromal fibroblasts existed in mouse Brca1-mutated mammary glands. HFD-induced obesity led to upregulated expression of extracellular matrix (ECM) genes (Col3a1, Col6a3, Eln, and Sparc) and downregulated expression of immunoregulatory genes (Iigp1 and Cxcl10) in these stromal subtype cells. These findings, taken together, suggest that obesity alters the ECM composition and immune ecosystem through modulating the functionality of mammary stromal fibroblasts. Moreover, scRNA-seq analysis of mammary immune cells indicated that HFD-induced obesity promoted the generation and/or recruiting of pro-tumorigenic M2 macrophages in mammary glands. Our studies provide new insight into a mechanistic paradigm wherein obesity modulates the functions of stromal and immune cells to create the tumorigenic microenvironment for promoting breast tumorigenesis.

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Reactome diagram viewer: data structures and strategies to boost performance

Cited by 139 publications

References 17 publications

Divergent Regulation of Myotube Formation and Gene Expression by E2 and EPA during In-Vitro Differentiation of C2C12 Myoblasts

Divergent Regulation of Myotube Formation and Gene Expression by E2 and EPA during In-Vitro Differentiation of C2C12 Myoblasts

CD36 and CD97 in Pancreatic Cancer versus Other Malignancies

Single-Cell RNA-seq Reveals Obesity-Induced Alterations in the Brca1-Mutated Mammary Gland Microenvironment

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